Anti-Mouse CD38 Antibody (NIMR5) is an anti-mouse CD38 IgG2a monoclonal antibody. Anti-Mouse CD38 Antibody (NIMR5) can activate the ERK signaling pathway and promote cell apoptosis. Anti-Mouse CD38 Antibody (NIMR5) can restore T cell function. Anti-Mouse CD38 Antibody (NIMR5) upregulates the expression of CD1d protein and enhances spleen cell proliferation, dendritic cell (DC) and natural killer T cell (NKT) expansion. Anti-Mouse CD38 Antibody (NIMR5) can be used for researches on cancer and immunology such as melanoma and colon cancer [1] [2] [3].
In Vitro, Anti-Mouse CD38 Antibody (NIMR5) (50 µg/mL, 4-12 h) induces ERK phosphorylation and promotes cell apoptosis in Ba/F3 cells and bone marrow B cell precursor[1]. Anti-Mouse CD38 Antibody (NIMR5) (1.0 μg/mL, 5-7 days) significantly inhibits the growth of tumor organoids MDOTS from wild-type female C57BL/6J mice bearing B16-ova tumors and BALB/c mice bearing CT26-GFP tumors combined with PD-1 mAb[2]. Anti-Mouse CD38 Antibody (NIMR5) (1 µg/mL, 6-48 h) significantly increases CD1d protein expression and has a synergistic effect with retinoic acid (RA) in THP-1 cells[3]. Anti-Mouse CD38 Antibody (NIMR5) (1 µg/mL, 4 days) enhances the proliferation of splenic cells and the expansion of dendritic cells (DC) and natural killer-T (NKT) cells induced by αGalCer, but have no significant effect on the production of cytokines (IL-4 and IFNγ)[3].
References:
[1]. Romero-Ramírez H, et al. CD38 expression in early B-cell precursors contributes to extracellular signal-regulated kinase-mediated apoptosis. Immunology. 2015 Feb;144(2):271-81.
[2]. Revach OY, et al. Overcoming resistance to immunotherapy by targeting CD38 in human tumor explants. Cell Rep Med. 2025 Jul 15;6(7):102210.
[3]. Chen Q, et al. All-trans-retinoic acid and CD38 ligation differentially regulate CD1d expression and α-galactosylceramide-induced immune responses. Immunobiology. 2015 Jan;220(1):32-41.
In Vitro, Anti-Mouse CD38 Antibody (NIMR5) (50 µg/mL, 4-12 h) induces ERK phosphorylation and promotes cell apoptosis in Ba/F3 cells and bone marrow B cell precursor[1]. Anti-Mouse CD38 Antibody (NIMR5) (1.0 μg/mL, 5-7 days) significantly inhibits the growth of tumor organoids MDOTS from wild-type female C57BL/6J mice bearing B16-ova tumors and BALB/c mice bearing CT26-GFP tumors combined with PD-1 mAb[2]. Anti-Mouse CD38 Antibody (NIMR5) (1 µg/mL, 6-48 h) significantly increases CD1d protein expression and has a synergistic effect with retinoic acid (RA) in THP-1 cells[3]. Anti-Mouse CD38 Antibody (NIMR5) (1 µg/mL, 4 days) enhances the proliferation of splenic cells and the expansion of dendritic cells (DC) and natural killer-T (NKT) cells induced by αGalCer, but have no significant effect on the production of cytokines (IL-4 and IFNγ)[3].
References:
[1]. Romero-Ramírez H, et al. CD38 expression in early B-cell precursors contributes to extracellular signal-regulated kinase-mediated apoptosis. Immunology. 2015 Feb;144(2):271-81.
[2]. Revach OY, et al. Overcoming resistance to immunotherapy by targeting CD38 in human tumor explants. Cell Rep Med. 2025 Jul 15;6(7):102210.
[3]. Chen Q, et al. All-trans-retinoic acid and CD38 ligation differentially regulate CD1d expression and α-galactosylceramide-induced immune responses. Immunobiology. 2015 Jan;220(1):32-41.